Wheel-Running Exercise Alleviates Anxiety-Like Behavior via Down-Regulating S-Nitrosylation of Gephyrin in the Basolateral Amygdala of Male Rats.

Physical exercise has beneficial effect on anxiety disorders, but the underlying molecular mechanism remains largely unknown. Here, it is demonstrated that physical exercise can downregulate the S-nitrosylation of gephyrin (SNO-gephyrin) in the basolateral amygdala (BLA) to exert anxiolytic effects. It is found that the level of SNO-gephyrin is significantly increased in the BLA of high-anxiety rats and a downregulation of SNO-gephyrin at cysteines 212 and 284 produced anxiolytic effect. Mechanistically, inhibition of SNO-gephyrin by either Cys212 or Cys284 mutations increased the surface expression of GABAAR γ2 and the subsequent GABAergic neurotransmission, exerting anxiolytic effect in male rats. On the other side, overexpression of neuronal nitric oxide synthase in the BLA abolished the anxiolytic-like effects of physical exercise. This study reveals a key role of downregulating SNO-gephyrin in the anxiolytic effects of physical exercise, providing a new explanation for protein post-translational modifications in the brain after exercise.

Reproductive Effect by Rheumatoid Arthritis and Related Autoantibodies.

Rheumatoid arthritis (RA) is a common inflammatory arthritis in women. The effects of RA on the reproductive system are usually overlooked, as RA is not diagnosed until later in reproductive age. Whether RA itself or its related rheumatoid antibodies have an impact on female reproductive function has long been a thought-provoking issue. In brief, relevant epidemiological evidence has shown that women affected by RA are more likely to have coexisting reproductive disorders, including infertility, endometriosis, and premature ovarian insufficiency (POI), or to subsequently develop them. Furthermore, linkage between RA and pregnancy loss (PL) as well as polycystic ovary syndrome (PCOS) is also well known, albeit controversial in available evidence. RA and reproductive disorders appear to share a similar inflammatory immune response and genetic background. The stress experienced by patients with RA may affect their reproductive choices to some extent. Notably, few studies have explored the impact of rheumatoid antibodies such as rheumatoid factors (RFs) and anti-citrullinated protein antibodies (ACPAs) on reproductive disorders. Although it has been mentioned that the rate of RF and/or ACPA positivity is higher in women with a history of PL and POI, the clinical relevance of this relationship and underlying mechanisms still need to be further clarified.

Improved mammalian family phylogeny using gap-rare multiple sequence alignment: A timetree of extant placentals and marsupials.

The timing of mammalian diversification in relation to the Cretaceous-Paleogene (KPg) mass extinction continues to be a subject of substantial debate. Previous studies have either focused on limited taxonomic samples with available whole-genome data or relied on short sequence alignments coupled with extensive species samples. In the present study, we improved an existing dataset from the landmark study of Meredith et al. (2011) by filling in missing fragments and further generated another dataset containing 120 taxa and 98 exonic markers. Using these two datasets, we then constructed phylogenies for extant mammalian families, providing improved resolution of many conflicting relationships. Moreover, the timetrees generated, which were calibrated using appropriate molecular clock models and multiple fossil records, indicated that the interordinal diversification of placental mammals initiated before the Late Cretaceous period. Additionally, intraordinal diversification of both extant placental and marsupial lineages accelerated after the KPg boundary, supporting the hypothesis that the availability of numerous vacant ecological niches subsequent to the mass extinction event facilitated rapid diversification. Thus, our results support a scenario of placental radiation characterized by both basal cladogenesis and active interordinal divergences spanning from the Late Cretaceous into the Paleogene.

α-MSH-catabolic enzyme prolylcarboxypeptidase in nucleus accumbens shell ameliorates stress susceptibility in mice through regulating synaptic plasticity.

Emerging evidence demonstrates the vital role of synaptic transmission and structural remodeling in major depressive disorder. Activation of melanocortin receptors facilitates stress-induced emotional behavior. Prolylcarboxypeptidase (PRCP) is a serine protease, which splits the C-terminal amino acid of α-MSH and inactivates it. In this study, we asked whether PRCP, the endogenous enzyme of melanocortin system, might play a role in stress susceptibility via regulating synaptic adaptations. Mice were subjected to chronic social defeat stress (CSDS) or subthreshold social defeat stress (SSDS). Depressive-like behavior was assessed in SIT, SPT, TST and FST. Based on to behavioral assessments, mice were divided into the susceptible (SUS) and resilient (RES) groups. After social defeat stress, drug infusion or viral expression and behavioral tests, morphological and electrophysiological analysis were conducted in PFX-fixed and fresh brain slices containing the nucleus accumbens shell (NAcsh). We showed that PRCP was downregulated in NAcsh of susceptible mice. Administration of fluoxetine (20 mg·kg-1·d-1, i.p., for 2 weeks) ameliorated the depressive-like behavior, and restored the expression levels of PRCP in NAcsh of susceptible mice. Pharmacological or genetic inhibition of PRCP in NAcsh by microinjection of N-benzyloxycarbonyl-L-prolyl-L-prolinal (ZPP) or LV-shPRCP enhanced the excitatory synaptic transmission in NAcsh, facilitating stress susceptibility via central melanocortin receptors. On the contrary, overexpression of PRCP in NAcsh by microinjection of AAV-PRCP alleviated the depressive-like behavior and reversed the enhanced excitatory synaptic transmission, abnormal dendritogenesis and spinogenesis in NAcsh induced by chronic stress. Furthermore, chronic stress increased the level of CaMKIIα, a kinase closely related to synaptic plasticity, in NAcsh. The elevated level of CaMKIIα was reversed by overexpression of PRCP in NAcsh. Pharmacological inhibition of CaMKIIα in NAcsh alleviated stress susceptibility induced by PRCP knockdown. This study has revealed the essential role of PRCP in relieving stress susceptibility through melanocortin signaling-mediated synaptic plasticity in NAcsh.

A thalamic circuit facilitates stress susceptibility via melanocortin 4 receptor-mediated activation of nucleus accumbens shell.

AIMS: Central melanocortin 4 receptor (MC4R) has been reported to induce anhedonia via eliciting dysfunction of excitatory synapses. It is evident that metabolic signals are closely related to chronic stress-induced depression. Here, we investigated that a neural circuit is involved in melanocortin signaling contributing to susceptibility to stress. METHODS: Chronic social defeat stress (CSDS) was used to develop depressive-like behavior. Electrophysiologic and chemogenetic approaches were performed to evaluate the role of paraventricular thalamus (PVT) glutamatergic to nucleus accumbens shell (NAcsh) circuit in stress susceptibility. Pharmacological and genetic manipulations were applied to investigate the molecular mechanisms of melanocortin signaling in the circuit. RESULTS: CSDS increases the excitatory neurotransmission in NAcsh through MC4R signaling. The enhanced excitatory synaptic input in NAcsh is projected from PVT glutamatergic neurons. Moreover, chemogenetic manipulation of PVTGlu -NAcsh projection mediates the susceptibility to stress, which is dependent on MC4R signaling. Overall, these results reveal that the strengthened excitatory neurotransmission in NAcsh originates from PVT glutamatergic neurons, facilitating the susceptibility to stress through melanocortin signaling. CONCLUSIONS: Our results make a strong case for harnessing a thalamic circuit to reorganize excitatory synaptic transmission in relieving stress susceptibility and provide insights gained on metabolic underpinnings of protection against stress-induced depressive-like behavior.

Repeated vagus nerve stimulation produces anxiolytic effects via upregulation of AMPAR function in centrolateral amygdala of male rats.

Repeated vagus nerve stimulation (rVNS) exerts anxiolytic effect by activation of noradrenergic pathway. Centrolateral amygdala (CeL), a lateral subdivision of central amygdala, receives noradrenergic inputs, and its neuronal activity is positively correlated to anxiolytic effect of benzodiazepines. The activation of ß-adrenergic receptors (ß-ARs) could enhance glutamatergic transmission in CeL. However, it is unclear whether the neurobiological mechanism of noradrenergic system in CeL mediates the anxiolytic effect induced by rVNS. Here, we find that rVNS treatment produces an anxiolytic effect in male rats by increasing the neuronal activity of CeL. Electrophysiology recording reveals that rVNS treatment enhances the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR)-mediated excitatory neurotransmission in CeL, which is mimicked by ß-ARs agonist isoproterenol or blocked by ß-ARs antagonist propranolol. Moreover, chemogenetic inhibition of CeL neurons or pharmacological inhibition of ß-ARs in CeL intercepts both enhanced glutamatergic neurotransmission and the anxiolytic effects by rVNS treatment. These results suggest that the amplified AMPAR trafficking in CeL via activation of ß-ARs is critical for the anxiolytic effects induced by rVNS treatment.

Study on Lung Injury Caused by Fine Particulate Matter and Intervention Effect of Rhodiola wallichiana.

Objective: The objective of this study was to observe the protective effect of Rhodiola wallichiana drops in a rat model of fine particulate matter (PM2.5) lung injury. Methods: Forty male Wistar rats were randomly divided into blank control (NC), normal saline (NS), PM2.5-infected (PM), and Rhodiola wallichiana (RW) groups. Rats in the NC group were not provided any interventions, whereas those in the NS and PM groups were administered normal saline and PM2.5 suspension by trachea drip once a week for four weeks. Rats in the RW group were intraperitoneally administered Rhodiola wallichiana for 14 days and then administered PM2.5 suspension by trachea drip 7 days after drug delivery. The levels of inflammatory factors such as interleukin-6, interleukin-1ß, and tumor necrosis factor-alpha and oxidative stress biomarkers such as 8-hydroxy-2'-deoxyguanosine, 4-hydroxynonenal, and protein carbonyl content were determined in the serum and bronchoalveolar lavage fluid by ELISA. The level of 4-hydroxynonenal in the lung was also determined using Western blotting and immunohistochemical staining. Results: Levels of inflammatory factors and oxidative stress biomarkers were all increased in the PM group but decreased in the RW group. Western blotting revealed increased 4-hydroxynonenal levels in the PM group but decreased levels in the RW group. Immunohistochemical staining also provided similar results. Conclusion: Rhodiola wallichiana could protect rats from inflammation and oxidative stress injury caused by PM2.5.

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter.

BACKGROUND Fine particulate matter (PM2.5) is the air pollutant that most threatens global public health. The purpose of this study was to observe the inflammatory and oxidative stress injury of multiple organs induced by PM2.5 in rats and to explore the tissue-protective effect of erdosteine. MATERIAL AND METHODS We randomly divided 40 male Wistar rats into a blank control group, a saline group, a PM2.5 exposure group, and an erdosteine intervention group. We assessed changes in organs tissue homogenate and biomarkers of inflammation and oxidative stress in serum and bronchoalveolar lavage fluid (BALF). RESULTS (1) The expressions of IL-6, IL-1ß, TNF-alpha, 8-OHdG, 4-HNE, and PCC in serum and BALF of the PM2.5 exposure group increased, but decreased after treatment with erdosteine, suggesting that erdosteine treatment attenuates inflammatory and oxidative stress injury. (2) The expression of γ-GCS in serum and lungs in the PM2.5 exposure group increased, but did not change significantly after treatment with erdosteine. This suggests that PM2.5 upregulates the level of γ-GCS, while erdosteine does not affect this protective response. (3) The expression of T-AOC in serum, lungs, spleens, and kidneys of the PM2.5 exposure group decreased, but increased after treatment with erdosteine. Our results suggest that PM2.5 can cause imbalance of oxidation/anti-oxidation in multiple organs, and erdosteine can alleviate this imbalance. CONCLUSIONS PM2.5 exposure can lead to inflammatory and oxidative stress damage in serum and organ tissues of rats. Erdosteine may be an effective anti-inflammatory and antioxidant that can reduce this injury.

IL-10 ameliorates PM2.5-induced lung injury by activating the AMPK/SIRT1/PGC-1α pathway.

Exposure to fine particulate matter with a diameter ≤2.5 µm (PM2.5) can cause a number of respiratory diseases. However, there is currently no safe treatment for PM2.5-induced lung damage. This study investigated the protective effect of IL-10 against lung injury and the possible involvement of AMPK/SIRT1/PGC-1α signaling. The mean diameter, particle size distribution, and zeta potential of PM2.5 samples were assessed using a Zetasizer Nano ZS90 analyzer. Thereafter, Wistar rats were exposed to PM2.5 (1.8, 5.4, or 16.2 mg/kg) alone or high-dose PM2.5 with recombinant rat IL-10 (rrIL-10; 5 µg/rat). Treatment with rrIL-10 ameliorated PM2.5-induced acute lung injury, reduced mitochondrial damage, and inhibited inflammation, oxidative stress, and apoptosis in the PM2.5-treated rats. Moreover, the mRNA and protein expression of AMPK, SIRT1, and PGC-1α were upregulated by rrIL-10 treatment. In conclusion, rrIL-10 protected lung tissues against PM2.5-induced inflammation by reducing oxidative stress and apoptosis via activating AMPK/SIRT1/PGC-1α signaling.

Continuous positive airway pressure versus mandibular advancement device in the treatment of obstructive sleep apnea: a systematic review and meta-analysis.

BACKGROUND: The goal of this study was to review relevant randomized controlled trials in order to determine the efficacy of continuous positive airway pressure (CPAP) versus mandibular advancement device (MAD) in the treatment of obstructive sleep apnea (OSA). METHODS: Using appropriate keywords, we identified relevant studies using PubMed, the Cochrane Library, and Embase. Key pertinent sources in the literature were also reviewed, and all articles published through October 2019 were considered for inclusion. For each study, we used odds ratios (ORs), mean difference (MD), and 95% confidence interval (95% CI) to assess and synthesize outcomes. RESULTS: We included 14 RCTs, for a total of 249 patients in the CPAP group and 247 in the MAD group. Compared with MAD, CPAP significantly decreased apnea hypopnea index (AHI) (WMD: -7.08, 95%CI: -9.06∼-5.10) and the percentage of stage 1 and 2 after therapy (WMD: -3.728, 95%CI: -6.912∼-0.543). However, compared with MAD, CPAP significantly decreased the SF-36-social function score (WMD: -3.381, 95%CI: -6.607∼-0.154).There was no significant difference in Epworth sleepiness scale score after therapy between the two groups. CONCLUSION: CPAP has better therapeutic efficacy in OSA patients than MAD.

lncRNA SCAL1 inhibits inducible nitric oxide synthase in lung cells under high-glucose conditions.

The lungs are one of the most common target organs of diabetic injury in patients with diabetes. Long non-coding RNA (lncRNA) smoke and cancer-associated lncRNA 1 (SCAL1), also known as lung cancer associated transcript 1 (LUCAT1), is known to have a pivotal role in lung cancer. The aim of the current study was to investigate the potential involvement of SCAL1 in diabetic lung disease. The expression levels of SCAL1 were determined by reverse transcription-quantitative PCR in serum samples from healthy controls (n=40), diabetic patients without lung disease (n=56) and diabetic patients with diabetic lung disease (n=44). Receiver operating characteristic analysis was used to evaluate the diagnostic value of serum SCAL1 in discriminating diabetic patients with diabetic lung disease from diabetic patients without lung disease and healthy controls. Pearson's correlation analysis was performed to examine the correlation between SCAL1 and inducible nitric oxide synthase (iNOS) mRNA expression levels in blood and lung tissue samples. Expression levels of iNOS and NO production following treatment with high (30 mM) glucose were examined by western blot analysis and NO assay, respectively. The expression levels of SCAL1 were significantly downregulated in diabetic patients with diabetic lung disease, and downregulated serum expression levels of SCAL1 effectively distinguished diabetic patients with diabetic lung disease from diabetic patients without lung disease and healthy controls. Treatment with high glucose significantly upregulated SCAL1 expression in normal lung cells. Furthermore, the overexpression of SCAL1 inhibited iNOS protein expression and reduced NO production in cells treated with high glucose. In conclusion, the current study demonstrated that lncRNA SCAL1 inhibits iNOS protein expression in lung cells under high-glucose conditions, which suggests that SCAL1 may have potential in the treatment of patients with diabetic lung disease.

Antagonistic Effects of N-acetylcysteine on Mitogen-activated Protein Kinase Pathway Activation, Oxidative Stress and Inflammatory Responses in Rats with PM2.5 Induced Lung Injuries.

Objective To evaluate the antagonistic effects of N-acetylcysteine (NAC) on mitogen-activated protein kinases (MAPK) pathway activation, oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter (PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups: blank control group (C1), water drip control group (C2), PM2.5 exposed group (P), low-dose NAC treated and PM2.5 exposed group (L), middle-dose NAC treated and PM2.5 exposed group (M), and high-dose NAC treated and PM2.5 exposed group (H). PM2.5 suspension (7.5 mg/kg) was administered tracheally once a week for four times. NAC of 125 mg/kg, 250 mg/kg and 500 mg/kg was delivered intragastrically to L, M and H group respectively by gavage (10 ml/kg) for six days before PM2.5 exposure. The histopathological changes and human mucin 5 subtype AC (MUC5AC) content in lung tissue of rats were evaluated. We investigated IL-6 in serum and bronchoalveolar lavage fluid (BALF) by Enzyme-linked immunosorbent assay (ELISA), MUC5AC in lung tissue homogenate by ELISA, glutathione peroxidase (GSH-PX) in serum and BALF by spectrophotometry, and the expression of p-ERK1/2, p-JNK1/2 and p-p38 proteins by Western blot. All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells. Rats receiving NAC treatment showed less histological destruction and mucus secretion. Of P, L, M and H group, MUC5AC in lung tissue, IL-6 in serum and BALF were higher than controls (C1 and C2) (all P<0.05), with the highest levels found in the P group and a decreasing trend with increase of NAC dose. The activity of GSH-PX in serum and BALF of PM2.5 exposed rats (P, L, M and H) was lower than that of controls (all P<0.05), with higher activities found in NAC treated rats (L, M, and H), and an increasing trend with increase of NAC dose. The expressions of p-ERK1/2, p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue (P, L, M and H) was higher than controls (all P<0.05), with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation, lung oxidative stress and inflammatory injury induced by PM2.5 in rats.

Predicting risk of pulmonary infection in patients with primary membranous nephropathy on immunosuppressive therapy: The AIM-7C score.

AIM: Pulmonary infection (PI) is the leading cause of death in patients with primary membranous nephropathy on immunosuppressive therapy. A rating score was thus developed to foresee the risk of PI in such patients. METHODS: We reviewed the charts of the pertinent patients treated during the past 3 years either with (n = 29) or without PI (n = 304). Clinical and laboratory data, the usage of cyclosporin A (CysA), and occurrence of PI were recorded. Cox regression analysis and receiver operating characteristic (ROC) curve were respectively used to identify the risk factors and assess their clinical relevance. RESULTS: The incidence of PI was 8.7% at 82.1 ± 20.9 days after the initiation of CysA regimen with a male predominance superimposed on smoking. Factors associated with PI were immunoglobulin G titer (hazard ratio = 4.56, 95% confidence interval = 2.31-8.95), plasma CysA concentration (3.71, 1.87-6.18), serum creatinine level (2.57, 1.31-5.82), CD4+ /CD8+ ratio (2.36, 1.26-6.06) and plasma albumin content (1.53, 1.05-3.25). These five factors, along with the male gender and smoking status, were granted different ratings after examined by the ROC curve and constituted the anticipating pulmonary infection in primary membranous nephropathy receiving CysA (AIM-7C) score. Accordingly, the respective percent composition of the infection and non-infection group was 0, 11.1%, 72.2%, 16.7% and 91.7%, 8.3%, 0, 0 in the order of low, moderate, high and utmost risk. Furthermore, eight new cases of PI were successfully predicted. CONCLUSION: Our AIM-7C score may therefore help to predict the onset and facilitate the prevention of PI, a potentially life-threatening complication of the immunosuppressive therapy.

TGF-β1/Smad signaling pathway in tissue fibrosis:research advances / 国际药学研究杂志

Transforming growth factor-β1(TGF-β1)is an important factor in tissue fibrosis. TGF-β1 directly ac- tivates Smad signaling which triggers the overexpression of profibrotic genes. A large number of studies have shown that the dysregulation of TGF-β1/Smad pathway is an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulators that promote TGF-β1-mediated tissue fibrosis,whereas Smad7 acts as a nega- tive feedback regulator of the TGF-β1/Smad pathway,blocking TGF-β1-mediated fibrosis. In addition,the recent re- searches have shown that microRNA(miRNA)can regulate the TGF-β1/Smad signaling pathway,and affect the process of tissue fibrosis. This article reviews the role of TGF-β1/Smad signaling pathway in renal,hepatic,pulmonary and myo- cardial fibrosis,as well as the regulation of TGF-β1/Smad signaling pathway by miRNA.

Effects of Lianhua Qingwen on Pulmonary Oxidative Lesions Induced by Fine Particulates (PM2.5) in Rats.

Objective To investigate the antagonistic effects of different doses of Lianhua Qingwen on pulmonary injury induced by fine particulates PM2.5 in rats. Methods Fine particulates suspended in the environment were collected. Forty-eight healthy adult wistar rats were randomly divided into 6 groups with 8 rats in each group. Four groups of rats were exposed to PM2.5 by intratracheally dripping suspensions of fine particulates PM2.5 (7.5 mg/kg) as dust-exposed model rats. Among them 24 rats in three groups received Lianhua Qingwen treatment (crude drug) at a dose of 2 g/kg, 4 g/kg, 8 g/kg per day for 3 days before dust exposure and were defined as low-dose, middle-dose and high-dose Lianhua Qingwen treatment groups respectively. The other dust-exposed model rats without treatment were assigned as PM2.5 control group. The un-exposed rats were set as saline control group (1.5 ml/kg saline) and blank control group. All rats were killed after 24 hours of the exposure. Lung tissue, serum and bronchoalveolar lavage fluid (BALF) were collected. The levels of malonaldehyde (MDA), lactate dehydrogenase (LDH), and glutathione peroxidase (GSH-PX) in blood serum and BALF, and superoxide dismutase (SOD) in blood surum were measured using fluorescent quantitation PCR; Expression of NF-E2-related factor 2(NRF-2), heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO1) in lung tissues were measured using Western blot. Pathological changes of lung tissues in each group were also examined. Results Pathology revealed thickened alveolar septum, congestion of capillary, interstitial edema and infiltration of lymphocyte and neutrophil surrounding bronchiole in the PM2.5 control group, which were significantly relieved in the Lianhua Qingwen treatment groups. Compared to the blank and saline control groups, the PM2.5 control group had significantly higher levels of LDH and MDA (p<0.01) and lower level of GSH-PS (p<0.01) in BALF, significantly higher levels of LDH and MDA (p<0.05) and lower level of GSH-PS (p<0.05) in rat serum. The levels of MDA in blood serum and BALF were significantly lower in each treatment group than that in PM2.5 control group (all P<0.05). In both middle-dose and high-dose treatment group the measurements of LDH in serum and BALF as well as GSH-PX in serum were significant difference from those of PM2.5 control group (all P<0.05). Expressions of NRF-2, HO-1 and NQO1 in lung tissues were significantly different among middle-dose and high-dose treatment group compared with those in PM2.5 control group (all P<0.05). Conclusion Fine particulates PM2.5 in environment may induce pulmonary oxidative lesions in rats. Middle-dose and high-dose Lianhua Qingwen has antagonist effece on the injuries induced by fine particulates.

Factors associated with future commitment and past history of human papilloma virus vaccination among female college students in northern Taiwan.

OBJECTIVE: To investigate factors influencing commitment to human papilloma virus (HPV) vaccination and prior vaccination among female college students in northern Taiwan. METHODS: A quota sample of 400 female college students was recruited from nine colleges in northern Taiwan during March 2013. Of these, 398 completed the self administered questionnaire which was designed based on the health promotion model. RESULTS: The results showed that factors associated with prior vaccination behavior were family history of gynecologic malignancy, ever being advised to get HPV vaccination, perceived barriers of action and perceived self-efficacy. Predictors for commitment to HPV vaccination in the next 6 months were the cost of vaccination, ever being advised to get HPV vaccination, perceived self-efficacy and situational influences. Perceived self-efficacy was significantly influenced by relationship status, past receipt of a recommendation for HPV vaccination and level of knowledge about HPV. CONCLUSION: When formulating vaccination policies, governmental or medical institutions should include these factors to promote vaccination.

Factors associated with future commitment and past history of human papilloma virus vaccination among female college students in northern Taiwan / 부인종양

OBJECTIVE: To investigate factors influencing commitment to human papilloma virus (HPV) vaccination and prior vaccination among female college students in northern Taiwan. METHODS: A quota sample of 400 female college students was recruited from nine colleges in northern Taiwan during March 2013. Of these, 398 completed the self administered questionnaire which was designed based on the health promotion model. RESULTS: The results showed that factors associated with prior vaccination behavior were family history of gynecologic malignancy, ever being advised to get HPV vaccination, perceived barriers of action and perceived self-efficacy. Predictors for commitment to HPV vaccination in the next 6 months were the cost of vaccination, ever being advised to get HPV vaccination, perceived self-efficacy and situational influences. Perceived self-efficacy was significantly influenced by relationship status, past receipt of a recommendation for HPV vaccination and level of knowledge about HPV. CONCLUSION: When formulating vaccination policies, governmental or medical institutions should include these factors to promote vaccination.

Clinical application of nateglinide:a Chinese expert consensus / 中华内分泌代谢杂志

Impaired eady phase insulin secretion is an important reason for leading to postprandial hyperglycemia.Nateglinide is a rapid-acting insulin secretagogue,which reduces postprandial blood glucose of type 2diabetic patient by restoring early phase insulin secretion.The efficacy and safety have been fully verified by clinical administration and it is more widely used to treat type 2 diabetic patients.Both sulfonylureas and glinides were named insulin secretagogue agents and regarded as alternative first-line drugs in the 2010 Chinese Guideline for treatment of type 2 diabetes.AACE/ACE Consensus statement claimed that glinides would be one of the important choices after metformin.In order to further guide the clinical application of nateglinide,16 national specialists in the field of endocrinology and metabolism of China discussed,drafted,and edited this consensus.The current consensus combined clinical evidences at home and abroad.systematically reviewed and summarized tlle results of these studies about nateglinide.It will provide guiding recommendations and reference concerning how to reasonably and effectively use nateglinide in the clinical practice.

Low serum testosterone and frailty in older men and women.

BACKGROUND: Frail older persons are at high risk of morbidity and mortality, and are characterized by body composition alterations. Serum testosterone, which regulates body composition, declines with age. We investigated the relation between serum testosterone level and physiological frailty in both older men and women. METHODS: This was a cross-sectional study of 108 adults 65 years old or older. Frailty status was determined by hand-grip strength, weight change, walking speed, exhaustion, and activity levels, and was classified as frail (3 or more deficits), pre-frail (1 or 2 deficits), or robust (no deficit) according to the Fried criteria. Serum total testosterone (TT) and sex-hormone-binding globulin were measured while free testosterone (FT) was estimated. RESULTS: Median (range) TT and FT were lower in frail than in pre-frail and robust men (TT: (frail) 15.7 [2.4-26.9] vs. (pre-frail) 19.4 [7.2-39.9] and (robust) 25.9 [13.2-35.2] nmol/L, P=0.03; FT: 230.0 [35.9-299.0] vs. 272.0 [86.7-411.0] and 303.0 [267.0-396.0] pmol/L, P=0.02) and women (TT: 0.31 [0.10-0.51] vs. 0.47 [0.14-1.55] and 0.45 [0.36-1.25] nmol/L, P=0.02; FT: 4.59 [0.46-6.63] vs. 4.66 [1.57-15.10] and 6.65 [3.91-21.00] pmol/L, P=0.03). After adjusting for age, comorbidities, body mass index, and serum albumin in ordinal logistic regression model, odds ratios of being frail were significantly higher for those participants whose TT and FT levels were in the lowest tertile compared to the highest tertile in men (TT: odds ratio [OR] 3.29, 95% confidence interval [CI] 1.14-9.50; FT: OR 3.44, 95% CI 1.05-11.22) and in women (TT: OR 6.69, 95% CI 1.84-24.31; FT: OR 4.86, 95% CI 1.31-18.08). CONCLUSIONS: Low serum testosterone levels were independently associated with frailty in the elderly Taiwanese.

Swedish and Chinese nurses' conceptions of ethical problems: a comparative study.

AIM: To investigate Swedish and Chinese nurses' conceptions of ethical problems and workplace stress and ascertain whether there are differences between the nurses in the two countries and between types of clinics. BACKGROUND: Nursing can be regarded as an ethical practice and ethical problems are one type of problems nurses have to deal with. DESIGN: The research design was comparative and quantitative. METHODS: A questionnaire was used. The study was carried out at one hospital in China and two hospitals in Sweden. One hundred and thirty-six Chinese nurses and 137 Swedish nurses participated. RESULTS: There was a statistical difference between nurses working in the different countries regarding commonest stated ethical problem. The Swedish nurses indicated a greater number of ethical problems than the Chinese nurses. The latter felt irritated, dissatisfied or sad at work or after work more often than the Swedish nurses. Forty-one per cent of the nurses in both countries thought there was a modest or rather big difference between the current and the desired quality of nursing. CONCLUSIONS: The findings were partially the same in the two countries and this underlines the importance of looking at ethical problems from an organisational perspective. RELEVANCE TO CLINICAL PRACTICE: The findings also show the need for a reduction of nurses' workload as well as the importance of assuring that nurses have the knowledge they need to carry out their work. The communication between nurses and other members of the health-care team, patients and relatives also needs to be improved.